Brain Atrophy in Alcoholics

  • E. González-Reimers
  • F. Santolaria-Fernández


Chronic alcoholics are at risk of developing several neurological alterations, such as the Wernicke–Korsakoff syndrome, the so-called alcoholic dementia, related to brain atrophy, cerebellar atrophy, and less frequently, the Marchiafava–Bignami syndrome, central pontine myelinolysis, and alcohol and tobacco-related amblyopia, in addition to the acute ethanol toxicity, various neurological syndromes related to withdrawal, and a higher incidence of stroke and head trauma. Although pathogenesis is still obscure, cytokine-mediated neuroinflammation and oxidative damage play a role in brain atrophy of uncomplicated alcoholics. In addition, thiamine deficiency, directly involved in the Wernicke–Korsakoff syndrome, and alterations in vitamins A, C, and, especially, vitamin E, related to oxidative damage, may contribute to brain damage. Iron excess, frequently observed in alcoholics, acting as a pro-oxidant, and deficiencies in selenium and zinc, involved in antioxidative capacity, have also been described as pathogenic factors, as is also the case of protein malnutrition, partly a consequence of poor nutrition and the irregular lifestyle of chronic alcoholics. Neuronal death by excitotoxicity, particularly related to binge-drinking episodes, is another mechanism responsible for neurocognitive impairment and brain atrophy in alcoholic patients. Finally, several reports also suggest that patients with chronic liver disease also present neurocognitive impairment independent of alcohol intake. Therefore, pathogenesis of this frequent complication of the alcoholic patient is multifactorial and incompletely understood.


Brain Atrophy Chronic Alcoholic Brain Damage Ethanol Consumption Thiamine Deficiency 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.



Alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid


Body mass index


Cyclic adenosine monophosphate


cAMP responsive element binding-protein


Computerized tomography


Desoxiribonucleic acid


Dual-energy x-ray absorptiometry




Gamma-amino-butyric acid






Magnetic resonance


Nuclear factor kappa B


Nicotinamide adenine dinucleotide phosphate


Reduced nicotinamide adenine dinucleotide




Tumor necrosis factor


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Copyright information

© Springer Science+Business Media, LLC 2011

Authors and Affiliations

  1. 1.Servicio de Medicina InternaHospital Universitario de CanariasLa LagunaSpain

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